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Differential microRNA editing may drive target pathway switching in human temporal lobe epilepsy. | LitMetric

AI Article Synopsis

  • * RNA editing, performed by ADAR proteins, can modify RNA and affect gene expression, but its impact on microRNAs in temporal lobe epilepsy has not been thoroughly investigated.
  • * This study identified significant editing in over 40 microRNAs, particularly miR-376a-3p, which showed altered levels and led to changes in gene expression linked to metabolism, highlighting the potential role of microRNA editing in the disease's pathophysiology.

Article Abstract

MicroRNAs have emerged as important regulators of the gene expression landscape in temporal lobe epilepsy. The mechanisms that control microRNA levels and influence target choice remain, however, poorly understood. RNA editing is a post-transcriptional mechanism mediated by the adenosine acting on RNA (ADAR) family of proteins that introduces base modification that diversifies the gene expression landscape. RNA editing has been studied for the mRNA landscape but the extent to which microRNA editing occurs in human temporal lobe epilepsy is unknown. Here, we used small RNA-sequencing data to characterize the identity and extent of microRNA editing in human temporal lobe epilepsy brain samples. This detected low-to-high editing in over 40 of the identified microRNAs. Among microRNA exhibiting the highest editing was miR-376a-3p, which was edited in the seed region and this was predicted to significantly change the target pool. The edited form was expressed at lower levels in human temporal lobe epilepsy samples. We modelled the shift in editing levels of miR-376a-3p in human-induced pluripotent stem cell-derived neurons. Reducing levels of the edited form of miR-376a-3p using antisense oligonucleotides resulted in extensive gene expression changes, including upregulation of mitochondrial and metabolism-associated pathways. Together, these results show that differential editing of microRNAs may re-direct targeting and result in altered functions relevant to the pathophysiology of temporal lobe epilepsy and perhaps other disorders of neuronal hyperexcitability.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10781512PMC
http://dx.doi.org/10.1093/braincomms/fcad355DOI Listing

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